Fig. 8
Proteinase K resistance of amyloid β peptide (Aβ) in human and mouse brain extracts. Human brain extracts of Alzheimer’s disease (AD), cerebral amyloid angiopathy (CAA), AD + CAA and less Aβ groups (A) as well as mouse brain extracts of R1.40 mice-AD, R1.40 mice-CAA, R1.40 mice-AD + CAA, R1.40 mice-less Aβ and R1.40 mice-PBS (B) were digested with 0, 25, 50, and 100 µg/mL of PK, and analyzed by Western blotting using antibodies against Aβ1–16 (6E10, 1:5,000) as the primary antibodies. In the human brain extracts, Aβ oligomers were digested by PK in all four groups (A). However, the signals of the Aβ monomers and dimers were different among the 4 groups; the signals of the Aβ monomers increased in the AD and AD + CAA groups, those of the Aβ dimers increased in the CAA group, and almost no signal of Aβ monomer and dimer signals were detected in the less Aβ group (A). On the other hand, in the mouse brain extracts, Aβ oligomers were digested and the signals of the Aβ dimers were lightly present (B)